Involvement of the different rat hippocampal glutamatergic receptors in development of seizures induced by soman: an autoradiographic study.

Glutamate (GLU)-receptor subtypes, (quisqualate (QA)-, kainate (KA)-, N- methyl-D-aspartate (NMDA)-receptors) and the phencyclidine sites localized in the ion-channel associated to the NMDA-receptors, were studied by autoradiography in the hippocampus of rats subjected to a convulsive dose of the acetylcholinesterase inhibitor soman (0-, 1,2,2-trimethylpropyl methylphosphonofluoridate). In intoxicated rats, a significant increase in L-[3H]-GLU binding occurred within the first 40 min of seizures in the hippocampal CA3 and CA1 areas. Whereas binding to KA- and NMDA-receptors remained unchanged, L-[3H]-GLU binding to CA3 QA-receptors increased by 31 and 50% respectively after 10 and 40 min of seizures. In CA1, the change in QA-receptors was delayed (+30% after 40 min) and accompanied by an increase in the phencyclidine site binding capacity, reflecting the probable concomitant opening of NMDA ion-channels. These findings confirmed the previously suspected involvement of GLU in the earliest stages of soman-induced seizures, and suggested that, in hippocampus, the primary activation of QA-receptors in the CA3 region could lead to the secondary recruitment of combined non-NMDA (QA) and NMDA mechanisms in CA1.